ArticleToxicology letters2014
Melanocytes and keratinocytes have distinct and shared responses to ultraviolet radiation and arsenic.
Article in Toxicology letters, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- Exposure to Trace Elements and Risk of Skin Cancer: A Systematic Review of Epidemiologic Studies.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2019Pooled it
- Genotype-Encoded UV Sensitivity in iPSC-Derived Human Melanocytes Reveals MX2 as a Physiological Amplifier of p53/p38-Mediated DNA Damage Signaling.International journal of molecular sciences · 2026Article
- Arsenic is a potent co-mutagen of ultraviolet light.Communications biology · 2023Article
- Arsenic and cancer: Evidence and mechanisms.Advances in pharmacology (San Diego, Calif.) · 2023Article
- Ambient UVR and Environmental Arsenic Exposure in Relation to Cutaneous Melanoma in Iowa.International journal of environmental research and public health · 2022Article
- Contribution of NADPH oxidase to the retention of UVR-induced DNA damage by arsenic.Toxicology and applied pharmacology · 2022Article
- Human Variation in DNA Repair, Immune Function, and Cancer Risk.Frontiers in immunology · 2022Review
- Viability of cultured human skin cells treated with 1,6-hexamethylene diisocyanate monomer and its oligomer isocyanurate in different culture media.Scientific reports · 2021Article
- Arsenic co-carcinogenesis: Inhibition of DNA repair and interaction with zinc finger proteins.Seminars in cancer biology · 2021Review
- NEnvironmental pollution (Barking, Essex : 1987) · 2020Article
- Peroxynitrite contributes to arsenic-induced PARP-1 inhibition through ROS/RNS generation.Toxicology and applied pharmacology · 2019Article
- Induction of retinal-dependent calcium influx in human melanocytes by UVA or UVB radiation contributes to the stimulation of melanosome transfer.Cell proliferation · 2017Article
- Inorganic arsenic inhibits the nucleotide excision repair pathway and reduces the expression of XPC.DNA repair · 2017Article
- Distinctive molecular responses to ultraviolet radiation between keratinocytes and melanocytes.Experimental dermatology · 2016Article
- Arsenic and ultraviolet radiation exposure: melanoma in a New Mexico non-Hispanic white population.Environmental geochemistry and health · 2016Article
- Selective Sensitization of Zinc Finger Protein Oxidation by Reactive Oxygen Species through Arsenic Binding.The Journal of biological chemistry · 2015Article
- MiR-21: an environmental driver of malignant melanoma?Journal of translational medicine · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The rise of melanoma incidence in the United States is a growing public health concern. A limited number of epidemiology studies suggest an association between arsenic levels and melanoma risk. Arsenic acts as a co-carcinogen with ultraviolet radiation (UVR) for the development of squamous cell carcinoma and proposed mechanisms include generation of oxidative stress by arsenic and UVR and inhibition of UVR-induced DNA repair by arsenic. In this study, we investigate similarities and differences in response to arsenic and UVR in keratinocytes and melanocytes. Normal melanocytes are markedly more resistant to UVR-induced cytotoxicity than normal keratinocytes, but both cell types are equally sensitive to arsenite. Melanocytes were more resistant to arsenite and UVR stimulation of superoxide production than keratinocytes, but the concentration of arsenite necessary to inhibit the activity of the DNA repair protein poly(ADP-ribose)polymerase and enhance retention of UVR-induced DNA damage was essentially equivalent in both cell types. These findings suggest that although melanocytes are less sensitive than keratinocytes to initial UVR-mediated DNA damage, both of these important target cells in the skin share a mechanism related to arsenic inhibition of DNA repair. These findings suggest that concurrent chronic arsenic exposure could promote retention of unrepaired DNA damage in melanocytes and act as a co-carcinogen in melanoma.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.